Figure 6
Figure 6. GA inhibits NF-κB activation induced by different molecules in NF-κB signaling pathway. (A) GA inhibited TNF-induced NF-κB–dependent reporter gene (SEAP) expression. A293 cells treated with the indicated concentrations of GA were transiently transfected with a NF-κB–containing plasmid linked to the SEAP gene. After 24 hours in culture with 0.1 nM TNF, cell supernatants were collected and assayed for SEAP activity. Results are expressed as fold activity over the activity of the vector control. (B,C) GA inhibited NF-κB–dependent reporter gene expression induced by TNF, TNFR1, TRADD, NIK, TRAF2, TAK1/TAB1, IKK, p65, and receptor-interacting protein (RIP). A293 cells were transiently transfected with the indicated plasmids along with a NF-κB–containing plasmid linked to the SEAP gene. Bars indicate standard deviation.

GA inhibits NF-κB activation induced by different molecules in NF-κB signaling pathway. (A) GA inhibited TNF-induced NF-κB–dependent reporter gene (SEAP) expression. A293 cells treated with the indicated concentrations of GA were transiently transfected with a NF-κB–containing plasmid linked to the SEAP gene. After 24 hours in culture with 0.1 nM TNF, cell supernatants were collected and assayed for SEAP activity. Results are expressed as fold activity over the activity of the vector control. (B,C) GA inhibited NF-κB–dependent reporter gene expression induced by TNF, TNFR1, TRADD, NIK, TRAF2, TAK1/TAB1, IKK, p65, and receptor-interacting protein (RIP). A293 cells were transiently transfected with the indicated plasmids along with a NF-κB–containing plasmid linked to the SEAP gene. Bars indicate standard deviation.

Close Modal

or Create an Account

Close Modal
Close Modal